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As a student nurse practitioner working within a medical assessment ward, I deal with a wide variety of patients who present with both acute and chronic conditions. This case study will identify the pathophysiology; look at the manifestations and clinical features of a condition. It will also discuss the therapeutic interventions and in turn evaluate the effectiveness of the interventions applied. Kyna (a pseudonym) was a forty-nine year old lady who was admitted to the ward for further investigations for a suspected deep vein thrombosis.

She had never been in hospital before and had no medical or surgical history other than the fact that she was clinically obese, with a body mass index of 32, and had been attending her GP for hormone replacement therapy as she was post-menopausal. It was also identified that Kyna had just returned from New York where she undertook an eight-hour flight. A deep vein thrombosis can be described by Anderson et al. 1999 as a clotting of blood in a deep vein of an extremity.

Weinmann et al 1994 states that a DVT is the result of a collection of intravascular cellular components, which consist of red, and white blood cells and some platelets bound together with fibrin strands. It usually occurs in the deep veins of the lower limbs as a result of slow blood flow and local activation of the blood clotting cascade and as a result of both local and systemic thrombogenic stimuli (Anand et al 1998). As discussed by Aquila (2001), in 1644, Schrnk first observed venous thrombosis when he described an occlusion in the inferior vena cava.

In 1846, a German pathologist, Rudolf Virchow recognised the association between venous thrombus in the legs and PE. He formulated the Virchow triad, which found that venous stasis, vessel wall injury and hypercoaguable state all related to thrombus formation. In other words, the development of venous thrombosis is best understood as the activation of coagulation in areas of reduced blood flow. Each of these will now be discussed in detail. In relation to blood flow, thrombus formation occurs when the natural antithrombotic mechanisms are overcome.

Furthermore, low pressures within the system complicate the haemodynamics. When a person stands upright, the hydrostatic pressure exceeds dynamic pressure impeding venous return. The action of the calf muscle pump overcomes this, which in turn can return the blood to the heart (Hirsch 1994). Laminar flow is also interfered with by clot formation. This promotes thrombus formation by bringing platelets into contact with the endothelium. Endothelial injury to blood vessels from a variety of sources is the most common cause of thrombus formation as stated by Cotran et al 1999.

Porth 2005 goes on to explain that the endothelial layer provides a smooth and slippery inner surface for the vessel, which prevents platelet adherence and blood clotting as long as it remains intact. The endothelial cells produce prostacyclin, which produces a number of vasoconstrictor substances; plasmin and endothelium derived relaxing factors, all of which are important inhibitors of intravascular coagulation. A venous catheter can be used as an example of a source of vascular injury where the endothelial lining is disrupted, resulting in increased fibrin strands gathering at the site of injury, allowing a clot to form.

Finally, hypercoagulability is the last element related to thrombus formation. White (2003) states that hypercoagulability is the condition in which an individual is at risk of but does not necessarily develop thrombosis. Basically, this means that it exists when coagulation overrides fibrinolysis. The coagulation pathway functions as a series of positive and negative feedback loops which control the activation process. In this case, the main aim of the pathway is to produce thrombin, which can then convert fibrinogen into fibrin, which in turn forms, a clot.

Porth 2005 explains that the coagulation process results from the activation of the intrinsic or extrinsic pathways. The intrinsic pathway begins in the blood itself whereas the extrinsic pathway, which is a much faster process, begins with trauma to the blood vessel or surrounding tissues and the release of the tissue factor. In both phases factor X is activated and prothrombin changes to thrombin, which acts as an enzyme to convert fibrinogen to fibrin, which stabilizes a clot. Thrombin also acts to produce an anticoagulant effect by forming an enzyme complex to activate protein C.

Other coagulation inhibitors are protein S and antithrombin, which activates thrombin directly (Guyton 2000). This is a slow process but can be accelerated by the binding of heparin. In relation to this case study, I will now look at the various assessments and investigations that were carried out and evaluate them. When considered alone, the individual clinical features of a DVT have a low predictive value. Wells 1997 stated that classic symptoms of a DVT include swelling, pain, and discolouration in the affected extremity.

Physical examination may reveal the palpable cord of a thrombosed vein, unilateral oedema, warmth and superficial venous dilation (Hyers 1999). Keron et al 1998 states that the clinical examination of patients with suspected DVT is often difficult because of the interplay between risk factors and the non-specific nature of the physical findings. In Kyna’s case, the Wells clinical tool (Wells et al 2006) was used initially. This tool is commonly used to predict the pretest probability of a DVT. It enables us to group patients to high, moderate, or low categories.

Combining this with the results of objective testing greatly simplifies the clinical workup of patients with suspected DVT. The Wells clinical prediction guide incorporates risk factors, clinical signs, and the presence or absence of alternative diagnosis. Koopman (1994) evaluated this clinical tool and concluded that it was the most valuable assessment tool used for assessing patients with a suspected DVT. Looking now at Kyna, using the Wells clinical tool, she had a score of two, which indicated that she had a moderate probability of having a DVT, therefore further investigations were necessary.

At this point it was necessary to take a D-dimer blood test. Bounameaux et al (1994) states that D-dimer fibrin fragments are present in a fresh fibrin clot. A D-dimer level may be elevated due to trauma, recent surgery, haemorrhage, cancer and sepsis. Therefore a D-dimer can only be used as a ‘rule-out’ test rather than a definite diagnosis. In Kyna’s case, the D-dimer result was greater than 2000 (normal values being 0- 250) so it was essential that an ultrasound was carried out to finally diagnose whether or not a DVT was present.

Compression ultrasonography is now the imaging test of choice to diagnose a DVT. Lack of compressibility of venous segment is the diagnostic criterion used, but the addition of Doppler can be useful to accurately identify vessels and to confirm a DVT (Heijboer et al 1993). It was concluded that ultrasonography was the best non-invasive diagnostic method in establishing a positive DVT showing 97% specificity and sensitivity (Molly 1996). In Kyna’s case it was now confirmed that there was a definite DVT in the left posterior tibial vein.

At this point, one may think it necessary to look at the patients’ history and maybe identify how Kyna developed a DVT. As she has no past medical or surgical history, it is important now to consider the predisposing factors along side any physiological changes that may have taken place. Daly et al 1996 found that an association between hormone replacement therapy (HRT) and DVT was evident. It was found to be a 2-3 fold increased risk of developing a DVT while being on oestrogen therapy. On top of this, Kyna was found to be clinically obese with a body mass index of 32.

Both the HRT and her clinical obesity would have increased venous stasis and increased the hypercoagulability, which is the homeostatic mechanism designed to increase clot formation. The other contributing factor to Kyna’s problem was that recently she had been on a long haul flight from New York. Looking at this particular aspect, it was identified that she would have been sitting for several hours without regularly moving her limbs. In fact Kyna stated that she had fallen asleep for the majority of the time on her flight home. The development of flight related deep vein thrombosis is multifactorial.

Due to the cramped crouch position in which Kyna would have been sitting in, would cause compression of the popiteal vein. Secondly, the immobility caused decreased amount of activity thereby a reduction in the muscle pump function (Scurr 2001). Both these factors increase the likelihood of stasis. The dry atmosphere within the air cabin coupled with a decreased fluid intake caused a haemoconcentration. This in particular related to Kyna because she did not drink anything while on the plane due to falling asleep for the majority of the journey.

Any consumption of alcohol or caffeine leads to diuresis, which further compounds the problem of haemoconcentration in the blood. The final insult is brought about by decreased air pressure and the presence of cabin hypoxia, due to the fact that the air within the cabin is recycled. All of this leads to a reduced fibrinolytic activity, an increased release of vein wall relaxin factors, promoting venous stasis, and finally leading to an increased stimulation of the coagulation cascade (Gertler et al 1993).

Recent documentation published by the Department of Health (2010) has emphasized the risk for women who are on HRT. It also stresses that the majority of air passengers do not need to take any medication to prevent DVT formation and those who are at risk, can simply reduce their chances by following simple exercises like exercising their calf muscle while seated. Treatment and prophylaxis for DVT formation is controversial. The primary objectives for the treatment of DVT are to prevent pulmonary embolism, reduce morbidity, and prevent or minimize the risk of developing the postphlebetic syndrome.

Effective, prompt treatment significantly decreases the likelihood of future episodes of DVT, which can occur in up to 33% of patients within five years (Turpie 1996). Anticoagulants are the main treatment used for patients with a confirmed DVT. Their aim is to prevent the extension and further formation of the thrombus and in turn reduce the risk of small portions of clot breaking off possibly causing a pulmonary embolism to occur. In Kyna’s case, two anticoagulants were administered. The first being enoxaparin, a low molecular weight heparin (LMWH), and secondly warfarin.

Haugh et al 1992 explains that LMWH has an action on antithrombin III (a coagulation factor) but due to its smaller weight, it has a longer half-life and it mainly inactivates factor Xa of the coagulation cascade. The LMWH’s have a lesser effect on thrombin, which inhibits the direct conversion of fibrinogen to fibrin than unfractionated heparin (Levine et al 1996). LMWH is given as a once a day daily dose and there is no need for regular blood level monitoring. Kyna’s therapeutic dose was based on her weight of 1. mg/kg on a once only dose. Once anticoagulation was achieved, warfarin was the drug of choice for long-term therapy to prevent clot recurrence. A standard warfarin protocol includes starting treatment at 10mg per day and titrating the dose every three to seven days to achieve an INR (international normalised ratio) between 2. 0 and 3. 0 (Crowther et al 1997). Ridker et al (2003) states that attempts have been made to maintain patients at an even lower INR (between 1. 5 and 2. 0), but results have been contradictory.

Warfarin acts by decreasing prothrombin and other procoagulation factors. It alters vitamin K such that it reduces its availability to participate in synthesis of the vitamin K-dependent coagulation factors in the liver. Warfarin is readily absorbed after oral administration. Its maximum effect takes 36 to 72 hours because of the varying half-lives of performed clotting actors. The plasma concentration of warfarin does not correlate with its anticoagulant activity therefore INR is used to assess control of anticoagulation.

Although there is some debate regarding the recommended length of warfarin therapy, the minimum recommended duration is 3 months (Hyers et al 2001). Prandoni et al (1996) states that study results indicate that treatment beyond 3 months is beneficial in patients who have a higher risk of recurrence. Schulman et al (1995), compared warfarin treatment durations of 6 weeks and 6 months, following patients for two years; a striking difference in the recurrence of thromboembilitic events in favour of extended treatment was observed. Results from this study demonstrated that patients who were treated with nticoagulants for 6 weeks were more than twice likely to experience recurrence of venous thromboembolism as patients who received 6 months of treatment. The incidence of recurrent thromboembolism was significantly lower in patients with permanent risk factors who were treated for 6 months. Another option, which could have been considered but was not used in Kyna’s case, was a catheter-directed fibrionlysis, in which a physician imbeds a catheter into the thrombus and infuses a fibrinolytic agent, avoiding the risks associated with systemic fibrinolytic therapy.

When anticoagulant therapy is contraindicated or causes complications, or in cases of recurrent DVT despite adequate anticoagulation, the physician may place an inferior vena cava filter to prevent thrombi from migrating into the lungs. Complications include puncture site bleeding; PE and inferior vena cava occlusion are rare if the filter has been properly placed. Mechanical means of DVT prophylaxis must also be taken into consideration. By applying TED stockings, they help by reducing the cross-sectional area within the calf muscles.

By doing so, there is an improvement of venous flow and an increased emptying of pockets of stasis. Pressure is greater at the dorsal venous plexus and is gradually decreased as one moves up the leg. There is strong evidence for the effectiveness of TED stockings. Agu (1999) analysed fifteen randomised trials showing that stockings decreased the risk of DVT by 64% in patients undergoing general surgical procedures. Similarly for passengers undergoing an airplane journey the stockings must be applied prior to boarding, and used until they are fully mobile.

The effects of above knee stockings are compromised when the knee is flexed in the ‘sitting position’. There are unfortunately complications with the use of stockings. They impair the oxygenation of tissues and a 10mmHg of pressure leads to a 10% reduction of blood flow. Compared with other agents TED stockings with the use of LMHW is much better than either stockings or Heparin alone. TED stockings should be removed regularly i. e. once daily, to assess the skin for redness or breakdown. Initially erythema and heat will be evident due to the inflammatory process taking place.

This is due to vascular changes in the inflammatory response, first vasoconstriction followed by vasodilatation of the arteriole. From a nursing perspective, it is important to ensure that the patient is comfortable by applying a cool pack to that particular area. Controversy exists regarding the role of ambulation in the therapy of DVT. The study by Partsch (2005) reviews the myths surrounding immediate ambulation and compression in the patient with the newly diagnosed DVT. The authors cited a number of studies that revealed a significant decrease in leg swelling and pain with early ambulation and compression.

In this particular case, Kyna was ambulatory from admission for the first twenty-four hours. In planning for discharge, it was vitally important to begin to educate Kyna about her DVT. She was advised about taking the HRT and the risks associated with it but decided to continue with her treatment She was also encouraged to engage in activity that will decrease the incidence of DVT, such as active leg exercises. With regards to her obesity, she was referred to a dietician and educated about the benefits of regular exercising.

Once again, Kyna was reluctant to see a dietician but did acknowledge the fact that she needed to exercise more regulalrly. Kyna was also advised to take adequate fluid intake to prevent dehydration and changes in the blood flow for future references. Finally Kyna was taught to lower the risk of developing a DVT in the future again by avoiding any constricting clothing on the legs that might decrease venous flow, sitting with knees bent or crossed for long periods and standing for long periods. Kyna was then discharged home the following day.

She was sent home on her oral anticoagulation therapy and was advised to inform her GP if she was intending going on any more flights in the future to enable her to get LMWH prophylaxis pre flight. In a patient feedback sheet, Kyna commented that her treatment was both effective and efficient, which makes the job of a student nurse practitioner very rewarding. In conclusion, it can be said that the pathophysiology of a deep vein thrombosis is best understood as the activation of coagulation in areas of reduced blood flow.

The three main factors linked to the development of a DVT are changes in blood coagulability, changes in vessel well and changes in blood flow. There is an association between air travel and deep vein thrombosis but there is currently no epidemiological evidence to support air travel as causation of DVT. Recognition and referral is necessary for correct diagnosis and prompt anticoagulation of patients. The sooner the treatment is started the more effective it will become. In turn this improved the patients prognosis leaving a very positive outcome.

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